RESUMEN
OBJECTIVE: To investigate the protective effect of total flavonoids from the leaves of Choerospondias axillaris (TFLC) on myocardial ischemia reperfusion injury (MIRI) model rats. METHODS: Male SD rats were randomly divided into sham operation group, model group, positive control group (verapamil, 0.02 g/kg), TFLC low-dose and high-dose groups (0.1, 0.4 g/kg), with 10 rats in each group. Administration groups were intragastrically given relevant medicine (2 mL/100 g); sham operation group and model group were given constant volume of normal saline intragastrically, once a day, for consecutive 7 d. After last medication, MIRI model was induced by modified ligation method. The times and duration of ventricular tachycardia (VT) and ventricular fibrillation (VF) in rats were recorded with biological function experiment system during reperfusion period.The activity of CK and contents of TNF-α, IL-6, NF-κB and NO in serum were determined by ELISA double antibody clip art assay. The morphological characteristics of myocardial tissue was observed by HE staining. The myocardial infarction scope (i.e. the ratio of myocardial tissue mass to ventricular mass) was measured by TTC method. RESULTS: Compared with sham operation group, the times and duration of VT and VF were increased or prolonged significantly in model group; CK activity, serum contents of TNF-α, IL-6 and NF-κB were enhanced or increased significantly, while NO content was decreased significantly (P<0.05 or P<0.01). Obvious myocardial infarction focus, serious cell structure damage, disorderly muscle fibers arrangement, cell nucleus pyknosis and accompanied inflammatory cell infiltration were all observed in cardiac tissue; the mass of infarcted myocardial tissue and ventricular as well as the scope of myocardial infarction increased significantly (P<0.01). Compared with model group, the times and duration of VT and VF were decreased or shortened significantly in administration groups; CK activity, serum contents of TNF-α, IL-6, NF-κB were decreased significantly, while NO content was increased significantly (P<0.05 or P<0.01). The above symptoms of myocardial injury were improved;the mass of infarcted myocardial tissue and ventricular as well as the scope of myocardial infarction was significantly reduced (P<0.05 or P<0.01). CONCLUSIONS: TFLC can relieve MIRI-induced ischemic arrhythmia and myocardial damage, reduce the release of inflammatory factors, promote the recovery of myocardial and endothelial cell function, reduce the scope of myocardial infarction and has a certain protective effect.